Carcinogenic bacteria

Short description: Bacteria known or suspected to cause cancer

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Bacteria involved in causing and treating cancers

Cancer bacteria are bacteria infectious organisms that are known or suspected to cause cancer.[1] While cancer-associated bacteria have long been considered to be opportunistic (i.e., infecting healthy tissues after cancer has already established itself), there is some evidence that bacteria may be directly carcinogenic. Evidence has shown that a specific stage in cancer can be associated with bacteria that is pathogenic.[2] The strongest evidence to date involves the bacterium H. pylori and its role in gastric cancer.[1]

Oncoviruses are viral agents that are similarly suspected of causing cancer.

## Contents

* 1 Known to cause cancer
* 1.1 Chronic inflammation
* 1.2 CagA
* 2 Speculative links
* 3 History
* 4 See also
* 5 References

## Known to cause cancer

Helicobacter pylori colonizes the human stomach and duodenum. It is described as a Class 1 carcinogen.[2] In some cases it can cause stomach cancer[3][4] and MALT lymphoma.[5] Animal models have demonstrated Koch's third and fourth postulates for the role of Helicobacter pylori in the causation of stomach cancer.[6] The mechanism by which H. pylori causes cancer may involve chronic inflammation, or the direct action of some of its virulence factors, for example, CagA has been implicated in carcinogenesis.[7] Another bacteria that is in this genus is Helicobacter hepaticus, which causes hepatitis and liver cancer in mice.[8]

### Chronic inflammation

Chronic inflammation contributes to the pathogenesis of several types of malignant diseases, but it is particularly important for H. pylori.[9] Following a H. pylori infection many circulating immune cells are recruited to the infection site including neutrophils.[10] To destroy the pathogens, neutrophils produce substances with antimicrobial activities such as oxidants like reactive oxygen species (ROS) and reactive nitrogen species (RNS).[11] H. pylori can survive the induced oxidative stress by producing antioxidant enzymes such as e.g., catalase.[12] However, the overproduction of ROS and RNS induces various types of DNA damage in the infected gastric cells.[12]At the same time H. pylori is known to down-regulate major DNA repair pathways.[13] As a result, genomic and mitochondrial mutations accumulate, leading to genomic instability - a well-known hallmark of Cancer [14] \- in the gastric cells.[13]

### CagA

The virulence factor CagA in H. pylori has been linked to the development of gastric cancer.[15] Once CagA is injected into the cytoplasm it can change the gastric cell signaling in both a phosphorylation-dependent and -independent manner.[11] Phosphorylated CagA affects cell adhesion, spread and migration[16] but can also induce the release of the proinflammatory chemokine IL-8.[15] Additionally, interactions of the CRPIA motif in non-phosphorylated CagA were shown to lead to the persistent activation of the PI3K/Akt pathway, a pathway that is often overly active in many human cancers.[17][18] This leads to the activation of the pro-inflammatory NF-κB and β-catenin pathways as well as increased gastric cell proliferation.[17] Furthermore, CagA has also been found to increase tumor suppressor gene hypermethylation and thereby inhibiting the tumor suppressor genes.[19] This is achieved by upregulating the methyltransferase DNMT1 via the AKT–NF-κB pathway.[19][20] Lastly, CagA also induces the expression of the enzyme spermine oxidase (SMOX) that converts spermine to spermidine.[11] As a by-product H2O2 is produced which causes ROS accumulation and contributes to the oxidative stress that the gastric cells experience during chronic inflammation.[11]

## Speculative links

A number of bacteria have associations with cancer, although their possible role in carcinogenesis is unclear.

Bacteria  | Suggested link

|

Salmonella Typhi, Paratiphi A, Typhimurium  | is associated with gallbladder cancer.[21][22]
Streptococcus bovis | is associated with colorectal cancer.[23][24]
Chlamydia pneumoniae | is associated with lung cancer.[23][25]
Mycoplasma | may also have a role in the formation of different types of cancer.[26][27]
Helicobacter pylori
Porphyromonas gingivalis | is associated with esophageal cancer, colorectal cancer, pancreatic cancer.[28]
Fusobacterium nucleatum | is associated with esophageal cancer, colorectal cancer, pancreatic cancer.[28]
Escherichia coli | is associated with colorectal cancer.[28]
Salmonella spp. | is associated with colorectal cancer.[28]
Enterotoxigenic Bacteroides fragilis | is associated with colorectal cancer.[28]
Chlamydia trachomatis in concert with HPV infection | is associated with cervical cancer.[28]
Streptococcus anginosus | is associated with esophageal cancer.[29]
Streptococcus mitis | is associated with esophageal cancer.[29]
Ruminococcus | is associated with colorectal cancer when under aerobic conditions.[30]

Salmonella Typhi has been linked to gallbladder cancer but may also be useful in delivering chemotherapeutic agents for the treatment of melanoma, colon and bladder cancer.[23] Bacteria found in the gut may be related to colon cancer but may be more complicated due to the role of chemoprotective probiotic cancers.[31] Microorganisms and their metabolic byproducts, or impact of chronic inflammation, may also be linked to oral cancers.[32]

The relationship between cancer and bacteria may be complicated by different individuals reacting in different ways to different cancers.[23]

## History

In 1890, the Scottish pathologist William Russell reported circumstantial evidence for the bacterial cause of cancer.[33] In 1926, Canadian physician Thomas Glover reported that he could consistently isolate a specific bacterium from the neoplastic tissues of animals and humans.[34] One review summarized Glover's report as follows:

> The author reports the isolation of a pleomorphic organism from various types of cancer which can be grown in pure cultures in its several phases. He produced a serum from it which has given remarkable results in a series of 50 reported cases. This is very important, if true. We suppose the Cancer Society will give an opinion later on the reliability of the findings."[35]

Glover was asked to continue his work at the Public Health Service (later incorporated into the National Institutes of Health) completing his studies in 1929 and publishing his findings in 1930.[36] He asserted that a vaccine or anti-serum manufactured from his bacterium could be used to treat cancer patients with varying degrees of success.[36] According to historical accounts, scientists from the Public Health Service challenged Glover's claims and asked him to repeat his research to better establish quality control.[37] Glover refused and opted to continue his research independently; not seeking consensus, Glover's claims and results led to controversy and are today not given serious merit.[38]

In 1950, a Newark-based physician named Virginia Livingston published a paper claiming that a specific Mycobacterium was associated with neoplasia.[39] Livingston continued to research the alleged bacterium throughout the 1950s and eventually proposed the name Progenitor cryptocides as well as developed a treatment protocol.[40] Ultimately, her claim of a universal cancer bacterium was not supported in follow up studies. In 1990 the National Cancer Institute published a review of Livingston's theories, concluding that her methods of classifying the cancer bacterium contained "remarkable errors" and it was actually a case of misclassification - the bacterium was actually Staphylococcus epidermidis.[38]

Other researchers and clinicians who worked with the theory that bacteria could cause cancer, especially from the 1930s to the 1960s, included Eleanor Alexander-Jackson, William Coley, William Crofton, Gunther Enderlein, Franz Gerlach, Josef Issels, Elise L'Esperance, Milbank Johnson, Arthur Kendall, Royal Rife, Florence Seibert, Wilhelm von Brehmer, and Ernest Villequez.[41] Alexander-Jackson and Seibert worked with Virginia Livingston. Some of the researchers published reports that also claimed to have found bacteria associated with different types of cancers.[42][43][44][45][46][47]

## See also

* List of oncogenic bacteria
* Infectious causes of cancer
* Chronic diseases and cancers linked to infectious microbes
* Oncovirus
* List of infectious diseases

## References

1. ↑ 1.0 1.1 "The Possible Role of Helicobacter pylori in Gastric Cancer and Its Management". Frontiers in Oncology 9. 22 February 2019. doi:10.3389/fonc.2019.00075. PMID 30854333.
2. ↑ 2.0 2.1 Cite error: Invalid `<ref>` tag; no text was provided for refs named `Khajuria_2015`
3. ↑ "Role of Helicobacter pylori infection and chronic inflammation in gastric cancer in the cardia". Japanese Journal of Clinical Oncology 37 (5): 365–369. May 2007. doi:10.1093/jjco/hym029. PMID 17578895.
4. ↑ "Helicobacter pylori and gastric cancer: the causal relationship". Digestion 75 (1): 25–35. 2007. doi:10.1159/000101564. PMID 17429205.
5. ↑ "Gastric MALT lymphoma and its relationship to Helicobacter pylori infection: management and pathogenesis of the disease". Microscopy Research and Technique 48 (6): 349–356. March 2000. doi:10.1002/(SICI)1097-0029(20000315)48:6<349::AID-JEMT5>3.0.CO;2-7. PMID 10738316.
6. ↑ "Helicobacter pylori infection induces gastric cancer in mongolian gerbils". Gastroenterology 115 (3): 642–648. September 1998. doi:10.1016/S0016-5085(98)70143-X. PMID 9721161.
7. ↑ "Helicobacter pylori CagA: a new paradigm for bacterial carcinogenesis". Cancer Science 96 (12): 835–843. December 2005. doi:10.1111/j.1349-7006.2005.00130.x. PMID 16367902.
8. ↑ "The complete genome sequence of the carcinogenic bacterium Helicobacter hepaticus". Proceedings of the National Academy of Sciences of the United States of America 100 (13): 7901–7906. June 2003. doi:10.1073/pnas.1332093100. PMID 12810954. Bibcode: 2003PNAS..100.7901S.
9. ↑ "Inflammation and cancer". Nature 420 (6917): 860–867. December 2002. doi:10.1038/nature01322. PMID 12490959. Bibcode: 2002Natur.420..860C.
10. ↑ "Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomes". Journal of Inflammation Research 8: 137–147. May 2015. doi:10.2147/JIR.S64888. PMID 26316793.
11. ↑ 11.0 11.1 11.2 11.3 "Helicobacter pylori and Gastric Cancer: Pathogenetic Mechanisms". International Journal of Molecular Sciences 24 (3): 2895. February 2023. doi:10.3390/ijms24032895. PMID 36769214.
12. ↑ 12.0 12.1 "Inflammation, DNA Damage, Helicobacter pylori and Gastric Tumorigenesis". Frontiers in Genetics 8: 20. 2017-02-27. doi:10.3389/fgene.2017.00020. PMID 28289428.
13. ↑ 13.0 13.1 "Helicobacter pylori infection generates genetic instability in gastric cells". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1806 (1): 58–65. August 2010. doi:10.1016/j.bbcan.2010.01.007. PMID 20122996.
14. ↑ "Hallmarks of cancer: the next generation". Cell 144 (5): 646–674. March 2011. doi:10.1016/j.cell.2011.02.013. PMID 21376230.
15. ↑ 15.0 15.1 "Helicobacter pylori CagA and gastric cancer: a paradigm for hit-and-run carcinogenesis". Cell Host & Microbe 15 (3): 306–316. March 2014. doi:10.1016/j.chom.2014.02.008. PMID 24629337.
16. ↑ "Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites". Proceedings of the National Academy of Sciences of the United States of America 99 (22): 14428–14433. October 2002. doi:10.1073/pnas.222375399. PMID 12391297. Bibcode: 2002PNAS...9914428H.
17. ↑ 17.0 17.1 "Helicobacter pylori CagA phosphorylation-independent function in epithelial proliferation and inflammation". Cell Host & Microbe 5 (1): 23–34. January 2009. doi:10.1016/j.chom.2008.11.010. PMID 19154985.
18. ↑ "The Pathogenic Role of PI3K/AKT Pathway in Cancer Onset and Drug Resistance: An Updated Review". Cancers 13 (16): 3949. August 2021. doi:10.3390/cancers13163949. PMID 34439105.
19. ↑ 19.0 19.1 "DNA methyltransferases and their roles in tumorigenesis". Biomarker Research 5 (1). December 2017. doi:10.1186/s40364-017-0081-z. PMID 28127428.
20. ↑ "Helicobacter pylori CagA induces tumor suppressor gene hypermethylation by upregulating DNMT1 via AKT-NFκB pathway in gastric cancer development". Oncotarget 7 (9): 9788–9800. March 2016. doi:10.18632/oncotarget.7125. PMID 26848521.
21. ↑ "Bacteria Moving into Focus of Human Cancer". Cell Host & Microbe 17 (6): 728–730. June 2015. doi:10.1016/j.chom.2015.05.016. PMID 26067598.
22. ↑ "Salmonella Manipulation of Host Signaling Pathways Provokes Cellular Transformation Associated with Gallbladder Carcinoma". Cell Host & Microbe 17 (6): 763–774. June 2015. doi:10.1016/j.chom.2015.05.002. PMID 26028364.
23. ↑ 23.0 23.1 23.2 23.3 "Bacteria and cancer: cause, coincidence or cure? A review". Journal of Translational Medicine 4 (1). March 2006. doi:10.1186/1479-5876-4-14. PMID 16566840.
24. ↑ "Association of Streptococcus bovis bacteremia with colonic neoplasia and extracolonic malignancy". Archives of Surgery 139 (7): 760–765. July 2004. doi:10.1001/archsurg.139.7.760. PMID 15249410.
25. ↑ "Chronic Chlamydophila pneumoniae infection in lung cancer, a risk factor: a case-control study". Journal of Medical Microbiology 52 (Pt 8): 721–726. August 2003. doi:10.1099/jmm.0.04845-0. PMID 12867569.
26. ↑ "[Mycoplasma infection and cancer]". AI Zheng = Aizheng = Chinese Journal of Cancer 23 (5): 602–604. May 2004. PMID 15142464.
27. ↑ "Persistent exposure to Mycoplasma induces malignant transformation of human prostate cells". PLOS ONE 4 (9). September 2009. doi:10.1371/journal.pone.0006872. PMID 19721714. Bibcode: 2009PLoSO...4.6872N.
28. ↑ 28.0 28.1 28.2 28.3 28.4 28.5 "Bacterial Infections and Cancer: Exploring This Association And Its Implications for Cancer Patients". International Journal of Molecular Sciences 24 (4): 3110. February 2023. doi:10.3390/ijms24043110. PMID 36834525.
29. ↑ 29.0 29.1 "Frequent and preferential infection of Treponema denticola, Streptococcus mitis, and Streptococcus anginosus in esophageal cancers". Cancer Science 95 (7): 569–574. July 2004. doi:10.1111/j.1349-7006.2004.tb02488.x. PMID 15245592.
30. ↑ "Major Anaerobic Bacteria Responsible for the Production of Carcinogenic Acetaldehyde from Ethanol in the Colon and Rectum". Alcohol and Alcoholism 51 (4): 395–401. July 2016. doi:10.1093/alcalc/agv135. PMID 26755640.
31. ↑ "Diet, anaerobic bacterial metabolism, and colon cancer: a review of the literature". Journal of Clinical Gastroenterology 39 (2): 98–109. February 2005. PMID 15681903.
32. ↑ "Exploring the link between microorganisms and oral cancer: a systematic review of the literature". Head & Neck 31 (9): 1228–1239. September 2009. doi:10.1002/hed.21140. PMID 19475550.
33. ↑ "An Address on a Characteristic Organism of Cancer". British Medical Journal 2 (1563): 1356–1360. December 1890. doi:10.1136/bmj.2.1563.1356. PMID 20753194.
34. ↑ "Progress in Cancer Research". Canada Lancet and Practitioner 67: 5. 1926.
35. ↑ "A selected public health bibliography with annotations". American Journal of Public Health 16 (12): 1242–1244. 1926. doi:10.2105/AJPH.16.12.1242.
36. ↑ 36.0 36.1 Glover TJ (1930). "The bacteriology of cancer". Canada Lancet and Practitioner 74: 92–111.
37. ↑ Studies in Malignancy. New York: Murdock Foundation. 1938.
38. ↑ 38.0 38.1 "Livingston-Wheeler therapy". CA 40 (2): 103–108. 1990. doi:10.3322/canjclin.40.2.103. PMID 2106368.
39. ↑ "Cultural properties and pathogenicity of certain microorganisms obtained from various proliferative and neoplastic diseases". The American Journal of the Medical Sciences 220 (6): 638–646. December 1950. doi:10.1097/00000441-195022060-00006. PMID 14789767.
40. ↑ "An experimental biologic approach to the treatment of neoplastic disease; determination of actinomycin in urine and cultures as an aid to diagnosis and prognosis". Journal of the American Medical Women's Association 20 (9): 858–866. September 1965. PMID 4220493.
41. ↑ Can Bacteria Cause Cancer?. New York: NYU Press. 1997. ISBN 978-0-8147-3562-6.
42. ↑ "Studies in Hodgkins Disease". Annals of Surgery 93 (1): 162–168. January 1931. doi:10.1097/00000658-193101000-00023. PMID 17866459.
43. ↑ Etude bacteriolgigue sur la maladie d'Hodgkin. Montpellier Medicine. June–August 1941.
44. ↑ "Siphonosopra polymorpha n. sp.: ein neuer microorganismus des blutes, seine beziehung zur tumorgenese". Med Welt 8: 1178–1185.
45. ↑ The True Nature of Viruses.. London, England: Staples Press Ltd.. 1936.
46. ↑ Le Parasitisme Latent des Cellules du Sang chez l' Homme, en Particulier dans le Sang des Cancreeux.. Paris, France: Librarie Maloine. 1955.
47. ↑ Eziopatogenese del Cancro. Milan, Italy: Amadeo Nicola.& c.. 1958.

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